Continued support is sought for the study of human and experimentally induced muscle disease by combined light, phase and electron-microscopic, as well as histochemical, and in selected instances immunocytochemical, electroncytochemical and biochemical methods. The study of the ultrastructural reactions of the muscle fiber organelles will be continued. Whenever possible, the ultrastructural observations will be quantitated by morphometric methods. Rare and hitherto undescribed diseases will be studied intensively by a variety of applicable morphologic, cytochemical and biochemical methods. The ultrastructure or normal and Duchenne dystrophy muscle cells grown in tissue culture will be investigated. Studies will be conducted on the ultrastructural localization of the acetylcholine receptor protein at the neuromuscular junction in human and experimental myasthenia gravis. The feasibility of the ultrastructural localization of immunoglobulin deposits at the neuromuscular junction in human and experimental myasthenia gravis will be explored. BIBLIOGRAPHIC REFERENCES: Engel, A.G., Angelini, C. and Nelson, R.A.: Identification of carnitine deficiency as a cause of human lipid storage myopathy. In: Exploratory Concepts in Muscular Dystrophy II. Excerpta Medica International Congress Series. 333:601-617, 1975. Boysen, G. and Engel, A.G.: Effects of microembolization on the skeletal muscle blood flow. Acta Neurol. Scandinav. 52:71-80, 1975.